Sneaking under the toxin surveillance radar: parasitism and sterol content

Abstract

Parasitic dinoflagellates of the genus Amoebophrya infect and kill bloom-forming dinoflagellates, including the toxic species Karlodinium micrum. Strains of K. micrum produce cytotoxic compounds (KmTX) that render cell membranes permeable to a range of small ions and molecules, resulting in cell death through osmotic lysis. Membrane sterol composition appears to play a role in the sensitivity of different algal species to the membrane-disrupting effects of KmTX. This sterol specificity also appears to be responsible for the apparent immunity of K. micrum to its own toxins. K. micrum has a unique sterol profile, shared only by the congeneric dinoflagellates Karenia brevis and K. mikimotoi, dominated by (24S)-4α-methyl-5α-ergosta-8(14), 22-dien-3β-ol (72% by weight). This sterol has recently been named gymnodinosterol. Analysis of the sterol content in Amoebophrya sp. infecting K. micrum showed gymnodinosterol also to be dominant (62%). This was not simply a reflection of retaining host lipid content because K. micrum contains octadecapentaenoic acid (18:5n3), largely in galactolipids of the chloroplast, whereas Amoebophrya sp. contained little to no 18:5n3. By having a sterol content similar to its host, Amoebophrya sp. is able to avoid cell lysis caused by the cytotoxic compounds produced by the host.